Mednotes

L12 I&I Lower respiratory infections

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tagsinfectionandimmunity, lecture
aliasesL12 I&I Lower respiratory infections

12 min read

Overview

This lecture covers respiratory tract infections from the pharynx down to the alveoli. It opens with two upper respiratory tract infections (URTIs), streptococcal pharyngitis and otitis media, then moves to lower respiratory tract infections (LRTIs): bronchitis/bronchiolitis, and pneumonia in its community-acquired, hospital-acquired/ventilator-associated, aspiration and immunocompromised-host forms. It closes with the laboratory approach to diagnosing URTI/LRTI. Throughout, the recurring distinction is typical vs atypical presentation and its link to whether an organism responds to penicillin.

Streptococcal pharyngitis

  • “Strep throat”, caused by Streptococcus Pyogenes (Group A Strep, GAS).
  • Accounts for 20-40% of pharyngitis in children, 5-15% in adults.
  • Epidemiology: typically ages 5-15 yrs, rare in children <3 or adults >40 yrs; Māori and Pacific Peoples affected across a much wider age range (3-43 yrs). Spread by respiratory droplets; risk raised by overcrowding, bed sharing, damp housing, limited healthcare access. Often secondary to a viral URTI or acquisition of a new strain.
  • Symptoms: acute sore throat, dysphagia, tender enlarged lymph nodes, patchy exudate (pus) on tonsils, petechiae on the palate, erythema of tonsils/pharynx.
  • Diagnosis: clinical (symptoms and risk factors) plus microbiological confirmation of GAS in risk groups (Gram stain, culture, point-of-care rapid antigen test), used to determine whether antimicrobials are appropriate.
  • Why treat: reduces risk of transmission and of two classes of complication:
    • Suppurative (direct tissue invasion): otitis media, sinusitis, peritonsillar abscess, sepsis.
    • Nonsuppurative (immune-mediated): rheumatic fever, rheumatic heart disease, acute glomerulonephritis.
  • Treatment: short course oral penicillin (amoxicillin or penicillin V) is the drug of choice; macrolides (e.g. azithromycin) if penicillin allergic, though resistance to macrolides exists.

Otitis media

  • Middle ear infection with inflammation and effusion in the middle ear space (MES); a very common childhood infection and a common reason children are given antimicrobials.
  • Epidemiology: 50% of children have had one infection by age 1, 90% by age 6; 33% of children have 6+ episodes by age 7. Peak incidence is in the first 2 years of life.
  • Risk factors: young age (no prior immunity, shorter/more horizontal eustachian tube (ET)); ET malformation (Down syndrome, cleft palate); socioeconomic factors (passive smoking, bottle-feeding, early cessation of breastfeeding); winter seasonality following viral URTI; overcrowding/damp housing (favours transmission of bacteria and viruses).
  • Aetiology: usually bacterial, from the nasopharyngeal microbiome - S. pneumoniae (most common), S. aureus (increasingly common), Haemophilus, Moraxella; S. pyogenes and gram-negative rods are less common causes. Viruses are also a common cause.
  • Pathogenesis: a preceding viral URTI causes inflammation that swells and occludes the ET, creating a vacuum in the MES; this draws in fluid (effusion), which is then colonised by bacteria from the nasopharynx.
  • Classification:
    • Acute otitis media (AOM): bacterial infection of the MES with purulent effusion; otalgia, otorrhoea, fever, often with a current/recent viral URTI; otoscopy shows opacity, bulging and erythema of the tympanic membrane.
    • Otitis media with effusion: no infection present, non-purulent effusion; follows AOM; recurrent episodes thicken the effusion (“glue ear”), impairing sound conduction and causing behavioural/learning problems; managed with tympanostomy (grommet) to drain the MES.
  • Diagnosis: mainly clinical (signs, symptoms, risk factors, otoscopy); microscopy/culture of effusion via tympanocentesis is possible but not routine.
  • Treatment: antimicrobial use is controversial, as >80% of children are cured with symptomatic treatment (analgesics) alone; amoxicillin +/- clavulanate is used, macrolides if penicillin allergy or resistance; vaccination against S. pneumoniae is preventive.

Bronchitis, bronchiolitis and the definition of pneumonia

  • Acute bronchitis/bronchiolitis in a previously well patient with no signs of severity is mostly viral, so antimicrobial treatment does not help.
  • Chronic bronchitis (COPD) exacerbations are often bacterial (Moraxella, S. pneumoniae, Haemophilus) and antimicrobials may help; sputum sampling is useful here.
  • Pneumonia is infection of the lung parenchyma (the alveoli) producing consolidation, i.e. inflammatory exudate filling the alveoli. Acute pneumonia is caused by bacteria or viruses; chronic pneumonia by fungi or TB.
  • Epidemiology: affects all age groups, more common in males; a leading cause of infection-related death, particularly in children under 5, adults over 65, and the chronically/terminally ill. Common in NZ, with Māori and Pacific Peoples disproportionately affected. WHO (2019): lower respiratory infections caused about 2.6 million deaths globally.

Routes of infection and clinical presentation of pneumonia

  • Routes microorganisms use to reach the lung:
    • Inhalation of aerosols - most common route in young/healthy people; associated with atypical pneumonia.
    • Aspiration of the normal URT/GIT microbiome - the most common route overall, especially in elderly/debilitated patients; associated with typical pneumonia.
    • Haematogenous spread - rare.
  • Typical presentation: productive cough (purulent sputum or haemoptysis), dyspnoea, fever/chills, pleuritic chest pain, rales/ronchi/crepitations/crackles, headache, fatigue, anorexia, nausea and vomiting. In the elderly, confusion, cyanosis and hypothermia may occur, and fever may be the only symptom.
  • Pathogenesis: an inflammatory process in the alveoli produces a fibrin-rich exudate with neutrophil/macrophage infiltration, replacing the normal open alveolar air spaces. Bacterial virulence factors include capsules (S. pneumoniae, Haemophilus, Klebsiella, E. coli, Pseudomonas, S. pyogenes, S. aureus) and toxins (pneumolysin in S. pneumoniae, PVL in S. aureus, exotoxin A in Pseudomonas).

Chest X-ray (CXR) patterns of pneumonia

  • Lobar: usually unilateral consolidation of a single lobe (multi-lobar/bilateral disease is more serious); classically the right lung; upper lobe in children/younger adults, middle/lower lobe in older adults; associated with S. pneumoniae.
  • Atypical pneumonia: often minimal or few signs on CXR (Mycoplasma, Chlamydia).
  • Bronchopneumonia: patchy, diffuse, small areas of consolidation, often bilateral; associated with Haemophilus and gram-negatives; seen in smokers, the elderly and COPD patients.
  • CXR pattern can suggest the likely cause and guide antimicrobial choice but is not always reliable, so other investigations are usually needed; CXR is not routine in CAP unless the patient is hospitalised.

Community-acquired pneumonia (CAP)

  • Definition: infectious pneumonia in a person who has not recently been hospitalised.
  • Risk factors: damage to ciliated epithelium (smoking, viral RTI); underlying disease (COPD, asthma, cystic fibrosis, lung cancer, heart disease); poor immune function (extremes of age, diabetes, cancer, organ transplant, asplenia); drugs (steroids, chemotherapy, alcohol abuse).
  • Typical bacteria: usually affect older people or those with comorbidities, produce typical symptoms/CXR signs, and typically respond to penicillin (historically).
    • Streptococcus pneumoniae: causes lobar pneumonia; can also affect previously healthy people.
    • Haemophilus influenzae: causes bronchopneumonia.
    • Moraxella: causes exacerbations of chronic bronchitis (COPD).
    • S. aureus (often post-influenza, PVL-positive strains): causes necrotising pneumonia - rapid, destructive, producing abscesses and empyema.
  • Atypical bacteria: Legionella, Mycoplasma pneumoniae, Chlamydia pneumoniae. These are intracellular or lack a cell wall, so they do not respond to penicillin (beta-lactam antibiotics), and they cause an absence of typical clinical/CXR signs.
    • Children/adolescents/younger adults: Mycoplasma/Chlamydia - vague, flu-like symptoms, minimal CXR signs, low-grade or absent fever, usually less severe disease.
    • Immunocompromised/elderly: Legionella (Legionnaires’ disease, covered in ELM3).

Hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)

  • HAP is defined as onset 48 hours or more after admission to a healthcare setting. US data: about 5% of hospitalised patients develop pneumonia; it accounts for 20% of healthcare-associated infections and is the leading cause of death from HAI (15% of hospital deaths), adding 7-9 days to admission and costing US$60,000-80,000 per patient.
  • VAP is HAP with onset 48-72 hours after endotracheal intubation; affects about 25% of ventilated patients, with incidence rising with duration of ventilation, and carries high mortality in at-risk patients.
  • Aetiology of VAP: gram-negative rods (Klebsiella, E. coli, Pseudomonas) account for over 50% of cases; also S. aureus, S. pneumoniae, Haemophilus, Legionella, Mycoplasma. Infections are often polymicrobial (mixed gram-positive/gram-negative), which complicates empiric therapy and often requires broad-spectrum or combination regimens. Antimicrobial-resistant organisms are a concern: MRSA, Pseudomonas, ESBL/carbapenemase-producing E. coli and Klebsiella.

Aspiration pneumonia

  • Results from aspiration of secretions from the upper respiratory tract, oesophagus or GI tract.
  • Risk factors: intubation/mechanical ventilation (disrupts natural barriers, gives direct access to the airway, allows retained secretions, risks equipment contamination); heart/lung/renal disease; abdominal surgery; decreased stomach acidity; abnormal lung secretions/clearance (e.g. cystic fibrosis, smoking); immunosuppression (diabetes, drugs, cancer, elderly).

Pneumonia in the immunocompromised

  • At-risk groups: transplant recipients, cancer patients, those on chemo/radiotherapy or steroids, diabetics, HIV/AIDS patients.
  • Decreased immunity increases both the risk of morbidity/mortality and the range of possible causative organisms: viruses (HSV, VZV, CMV), fungi (Candida, Aspergillus, Pneumocystis, Mucoraceae), mycobacteria (M. tuberculosis, M. avium), and typical/atypical bacteria.
  • Invasive fungal infection (e.g. Aspergillus, Mucoraceae): environmental spores are inhaled, causing URTI/LRTI; the fungi can invade blood vessels and disseminate to the brain, gut, liver, spleen and kidneys. Treatment is IV amphotericin B, sometimes with surgery, but prognosis is poor.

Laboratory diagnosis of respiratory tract infection

  • For bacterial pneumonia (typical causes): sputum culture and Gram stain are the mainstay, sampled before antimicrobials are started so results can direct choice of therapy; early morning samples are preferred as secretions are more concentrated.
  • If sputum cannot be obtained/cultured: blood culture, pleural fluid or bronchoalveolar lavage (BAL) can be used, and are the main options when atypical causes are suspected since these organisms do not Gram stain and are difficult to culture.
  • Molecular methods (PCR) are used to detect atypical causes.
  • Antimicrobial sensitivity testing (AST) is important given common resistance in respiratory pathogens, supporting a choice between empiric and narrow-spectrum (stewardship) therapy.
  • Procalcitonin helps differentiate bacterial from viral pneumonia, and so helps determine whether antimicrobials are appropriate.
  • Gram stain is also used for streptococcal pharyngitis and otitis media diagnosis (see relevant sections above); point-of-care rapid antigen testing is specific to strep pharyngitis.

Self-test

  1. Define pneumonia in terms of the underlying lung pathology, and state how acute and chronic pneumonia differ in the type of organism responsible.
  2. Distinguish typical from atypical pneumonia in terms of response to penicillin, and explain why atypical organisms behave this way.
  3. Describe the three routes by which microorganisms reach the lung in pneumonia, and state which route is most common overall and which pneumonia type it is associated with.
  4. List the three CXR patterns of pneumonia described, with one distinguishing radiological feature and a typical causative organism for each.
  5. Distinguish community-acquired pneumonia (CAP) from hospital-acquired pneumonia (HAP), including the time threshold that defines HAP.
  6. Describe, in steps, the pathogenesis of otitis media following a viral URTI.
  7. Distinguish acute otitis media (AOM) from otitis media with effusion.
  8. List the diagnostic approaches used for streptococcal pharyngitis and state what treatment of it is trying to prevent.
  9. Distinguish the suppurative from the nonsuppurative complications of untreated streptococcal pharyngitis, giving an example of each.
  10. What is the first-line treatment for streptococcal pharyngitis, and what is substituted in penicillin allergy?
  11. Describe the epidemiology of ventilator-associated pneumonia (VAP): how it is defined by timing, what proportion of ventilated patients it affects, and what increases its incidence.
  12. A ventilated ICU patient develops fever and purulent sputum 4 days after intubation. What is the likely diagnosis, and what feature of its aetiology complicates the choice of empiric antimicrobial therapy?
  13. Describe how the range of pathogens causing pneumonia differs in an immunocompromised host compared with an immunocompetent host.
  14. Describe the pathogenesis and treatment of invasive pulmonary fungal infection in an immunocompromised patient.
  15. A previously well young adult presents with a dry cough, low-grade fever and minimal CXR changes; an elderly nursing-home resident presents with rapid-onset fever and unilateral lobar consolidation. Explain the likely difference in causative organism and route of infection between the two cases.

Answers

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